Background: Physiologic studies in rodents and preliminary human studies have suggested that Roux-en-Y gastric bypass (RYGB) improves type 2 diabetes mellitus (T2DM) by way of metabolic changes, long before the bariatric or weight loss effects occur, leading to the concept of "metabolic surgery." To test this hypothesis, we studied patients with insulin-dependent T2DM who underwent RYGB to determine whether T2DM remission in this treatment-resistant subgroup occurred independent of weight loss.
Methods: Of all the patients undergoing RYGB from 2000 to 2006 (n = 1546) with >/=12 months of follow-up, 318 had T2DM (21%), and 75 (24%) of these were insulin dependent. Of the 75 patients, 4 were found to have T1DM (5.3%) and were excluded, leaving a study population of 71 patients. The patients who achieved remission, defined as a cessation of diabetic medications with a hemoglobin A1c level of <7%, were compared with those who did not achieve remission. Statistical significance was set at P < .05, using the Student t test, chi-square test, and logistic regression analysis, as appropriate.
Results: After RYGB, all 71 patients with insulin-dependent T2DM had achieved a reduction in the dose and/or number of medications at 29.6 +/- 17.0 months. Of these 71 patients, 35 (49%) demonstrated a remission of T2DM. The preoperative body mass index, age, number of medications, and hemoglobin A1c level did not differentiate between those who attained remission and those who still required diabetic medication. From the multivariate analysis, the significant factors associated with remission were the preoperative insulin dose and the percentage of excess weight loss. The percentage of excess weight loss was greater in the remission patients as early as 3 months postoperatively (P = .04) and also at 6, 12, 18, and 24 months.
Conclusion: RYGB uniformly improved the medication requirements of patients with insulin-dependent T2DM. Although physiologic mechanisms likely contributed, early rapid weight loss was associated with the remission of T2DM.